Navicular disease, also referred to as Podotrochlosis or Podotrochlitis, is essentially a chronic degenerative condition of the Navicluar bursa and the Navicular bone. This condition involves damage to the flexor surface of the bone and to the overlying deep digital flexor tendon, with osteophyte formation on the lateral and proximal borders of the bone. The syndrome has a complex pathogenesis with a heretofore unknown disease origin. It afflicts primarily the forefeet of horses and is essentially unknown in ponies or donkeys. Either Haemophilus somnus (H. somnus) or Histophilus ovis (H. ovis) or both is/are the putative cause(s) of Navicular disease in horses. Both organisms are gram negative, non-motile, non-spore forming, pleomorphic coccobacilli. H. ovis, an organism commonly found in sheep, is closely related to H. somnus. Haemophilus agni (H. agni) is another member of the Haemophilus genus that is virtually indistinguishable from H. somnus. Therefore, these antigens specific to H. agni may also prove beneficial in the treatment and/or prevention of Navicular disease.
H. somnus causes infectious thromboembolic meningitis (TEME) in cattle. Preparations of H. somnus bacterin have been used prophylactically to prevent TEME. H. somnus circulates in the bloodstream of the infected animal and can cause severe vasculitis, hemorrhage, thrombosis and/or infarction in many of the afflicted animal's organs. Thrombosis is an intravascular blood clot found at the point of its origin. All or part of a thrombosis may break off the vessel and be carried through the blood stream as an embolus. The embolus may lodge distally at a narrow point in the animal's vasculature further resulting in either an aneurysm or edema.
Examination of horses afflicted with Navicular disease reveals degenerative lesions in the Navicular bone and changes in the shape of the vascular channels supplying nutrients to the bursa and Navicular bone. This disease pathology may occur due to embolism blockage of the Navicular bone's vasculature, which creates edema in the bursa. Bursa edema places pressure on the surrounding nerves, inducing pain in the horse's hoof, which may further result in lameness in the afflicted animal.
Navicular disease initially manifests itself as intermittent lameness, shortened strides, and a possible tendency to stumble. An afflicted horse relieves the pressure of the deep flexor tendon on the painful area by pointing or advancing the affected foot, with the heel off the ground, resulting in the animal's altered gait. Radiographs of the hoof will further reveal degenerative lesions in the Navicular bone, with a change in shape of the vascular channels from their normal hair-line appearance to a triangular or inverted flask shape. Such lesions may result from either aging or onset of disease and must be interpreted in light of the animal's history and other clinical findings.
Navicular disease is both chronic and degenerative. Use of this novel process will prevent further Navicular disease related degeneration of the bursa. Hoof degeneration as a result of Navicular disease often times leads to euthanizing the animal. Until this novel therapy, Navicular disease was incurable with only palliative measures available for treatment of the afflicted animal. This treatment should vastly prolong the life and usefulness of horses afflicted with this disease.
The treatment of the present disclosure is a preventative for the development of this disease. In a horse which is otherwise unmarked by this disease, administration of this treatment serves as a preventative, i.e., vaccination. It provides what is thought to be fairly long protection. By that, the protection from a single vaccination is some number of months, but it is conjectured that the protection can be extended with periodic renewals. It may be that sufficient protection is achieved in a healthy adult horse after three to six spaced vaccination dosages that lifetime immunity is achieved. However, the outside limit of that duration is not yet fully known in the absence of conducting life time tests which would implicate many years of testing and observation.
In another aspect of the present disclosure, the Navicular disease is arrested by administration of the vaccination procedure set forth in this disclosure. Assume that an adult horse has the onset of a Navicular disease. As soon as some lameness is noted, and upon examination including radiographs as appropriate, the vaccination procedure is then started. A series of treatments is administered as will be described. Ultimately, the horse is treated some number of times sufficient to arrest the Navicular disease. Assume for purposes of discussion that the onset of the disease damaged the flexor surface of the bone. Assume that this amounts to about 20% of that surface. As a generalization, this treatment will stop the further degeneration of the joint. The further progression of the Navicular disease and the resultant degeneration is arrested. If it is caught in time, the animal can be restored to usefulness and can be brought to a state where the animal is substantially free of the disease. Accordingly, disease progress is limited. While it is not shown yet that regeneration occurs, further degradation is stopped. It is believed that this will substantially extend the useful life of diseased horses so that, even though injured, they still have some relative mobility. Lameness as a result of the affliction is capped.
Navicular disease is distinguishable from other diseases affecting the bursa and Navicular bone, such as ringbone (by definition, located at another joint). The treatment disclosed in these claims will not prevent onset or progression of other degenerative joint diseases including chronic osteoarthritis, ringbone, or spavin, which have different physiological origins. Faulty conformation, repeated trauma to the Navicular bone and bursa, and undue stress are the rather common factors contributing to joint degeneration in horses (e.g., ringbone).
The treatment in accordance with present disclosure uses a standard level of potency of a medication which is sometimes known as Somnugen (a trademark of BIOCEUTIC). Potency of the treatment will be discussed below. In general terms, the product known as Somnugen and Bar Somnus are prepared from highly immunogenic strains of Haemophilus somnus. The potent vaccine is administered in the fashion set forth below.
The injections are administered deep (1 1/2 20 g. needle) intramuscular in the neck of the horse. The injections must be low in the ventral region as drainage may be necessary due to abscess formation. Different injection sites in the neck (both sides) are mandatory because of the soreness and swelling which may or may not occur. The stage of the disease seems to have an effect upon the occurrences of swelling and/or soreness. Usually the injection site becomes sore and swollen as do the front feet. The soreness/swelling lasts (depending upon the disease stage) for approximately three to four days. The formation of an abscess at the injection site is repressed by adherence to stringent aseptic techniques. Specific intramuscular injections are definitely necessary. Needle cannulae are to be massaged to prevent vaccine from coming back up to the subdermal area post vaccination.
After one treatment, and to especially aggressively deal with an adult horse which is known to have the Navicular disease, the treatment regimen is repeated. After the first injection, the horse will have sore front feet and a very sore and warmer than usual injection site within 24 to 48 hours post first injection. If not, then the presence of Navicular disease should be questioned. Remember that the soreness may or may not occur when the vaccine is being used as a prophylactic measure and may or may not occur after the 6-month booster vaccination. After an interval, a second injection is given, again ideally in the neck but a different injection site following the same procedure as applied to the first injection. A course of treatment for an adult horse involves six treatments. They are spread over a span of six weeks in the preferred sequence to a longer interval of perhaps 50% longer. When six treatments are administered in six weeks, that basically involves one week spacing between treatments.
After stopping the onset of the active disease, it is sound wisdom to continue with maintenance or booster shots thereafter periodically, for instance one per year. Again, this would require data over the lifetime of many adult horses for which data have not been accumulated.